A global regulator of secondary metabolite production in Pseudomonas fluorescens Pf-5

Corbell, Nathan; Loper, Joyce E.

doi:10.1128/jb.177.21.6230-6236.1995

Cited by 145 publications

(109 citation statements)

References 42 publications

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“…The secondary metabolites HCN and protease, as well as phloroglucinol, are known to be under similar global control from a two component system in P. fluorescens (Corbell & Loper, 1995 ;Dunne et al, 1996). Strain F113(pBSL-8), in which phloroglucinol production was repressed, and the F113-phlF -mutant were assessed in their production of the HCN and protease metabolites by plate assays, as described in Methods.…”

Section: Phlf Does Not Have a Repressive Effect On Other Secondary Mementioning

confidence: 99%

Regulation of production of the antifungal metabolite 2,4-diacetylphloroglucinol in Pseudomonas fluorescens F113: genetic analysis of phlF as a transcriptional repressor The GenBank accession number for the sequence reported in this paper is AF129856.

et al. 2000

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The antifungal metabolite 2,4-diacetylphloroglucinol plays a major role in the biocontrol capabilities of Pseudomonas fluorescens. The phloroglucinol biosynthetic locus of P. fluorescens F113 has been isolated previously. From nucleotide sequence data, a putative regulator gene (phlF) was identified upstream and divergently transcribed from the phlACBD phloroglucinol biosynthetic genes. PhlF shows similarity to various transcriptional repressors in the EMBL database and exhibits a helix-turn-helix motif in its amino acid sequence. phlF was cloned into an expression vector and the PhlF protein product was purified. Gel retardation experiments demonstrated PhlF to be a DNA-binding protein and showed that it binds to the phlA-phlF intergenic region. Introduction of phlF into P. fluorescens F113 in multiple copies resulted in repression of phloroglucinol production in this strain. This effect was mediated at the transcription level since the expression of a phloroglucinol biosynthetic gene fusion in this background was equally repressed. Furthermore, the inactivation of phlF results in derepression of phloroglucinol production in this strain.

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Section: Phlf Does Not Have a Repressive Effect On Other Secondary Mementioning

confidence: 99%

Regulation of production of the antifungal metabolite 2,4-diacetylphloroglucinol in Pseudomonas fluorescens F113: genetic analysis of phlF as a transcriptional repressor The GenBank accession number for the sequence reported in this paper is AF129856.

et al. 2000

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“…The cognate sensor appears to be the transmembrane protein LemA (Hrabak and Willis, 1992;Rich et al, 1994). Both the gacA and lemA genes are highly conserved in fluorescent pseudomonads (Liao et al, 1994;Corbell and Loper, 1995;Grewal et al, 1995). In Salmonella typhimurium, the gacA homologue sirA is essential for invasion and virulence (Johnston et al, 1996), and a gacA homologue is also known to be present in Escherichia coli (Moolenaar et al, 1987) and in Erwinia carotovora (Eriksson et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

The global activator GacA of Pseudomonas aeruginosa PAO positively controls the production of the autoinducer N‐butyryl‐homoserine lactone and the formation of the virulence factors pyocyanin, cyanide, and lipase

Reimmann

Beyeler

Latifi

et al. 1997

Molecular Microbiology

399

349

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SummaryThe global activator GacA, a highly conserved response regulator in Gram-negative bacteria, is required for the production of exoenzymes and secondary metabolites in Pseudomonas spp. The gacA gene of Pseudomonas aeruginosa PAO1 was isolated and its role in cell-density-dependent gene expression was characterized. Mutational inactivation of gacA resulted in delayed and reduced formation of the cell-density signal N-butyryl-L-homoserine lactone (BHL), of the cognate transcriptional activator RhlR (VsmR), and of the transcriptional activator LasR, which is known to positively regulate RhlR expression. Amplification of gacA on a multicopy plasmid caused precocious and enhanced production of BHL, RhlR and LasR. In parallel, the gacA gene dosage markedly influenced the BHL/RhlR-dependent formation of the cytotoxic compounds pyocyanin and cyanide and the exoenzyme lipase. However, the concentrations of another known cell-density signal of P. aeruginosa, N-oxododecanoyl-L-homoserine lactone, did not always match BHL concentrations. A model accounting for these observations places GacA function upstream of LasR and RhlR in the complex, cell-density-dependent signal-transduction pathway regulating several exoproducts and virulence factors of P. aeruginosa via BHL.

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“…The response-regulator GacA and the corresponding sensor LemA are components of a highly conserved signal pathway within the genus Pseudomonas (Gaffney et al, 1994;Rich et al, 1994;Corbell & Loper, 1995;Haas & Carruthers, 1996, Université de Lausanne, Switzerland, personal communication). GacA is a response regulator in the Fix-DegU family of two-component regulatory systems Gaffney et al, 1994) and a conserved regulator of virulence factors in Pseudomonas aeruginosa (Rahme et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

**The global regulator GacA of Pseudomonas fluorescens CHA0 is required for suppression of root diseases in dicotyledons but not in Gramineae**

1997

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Pseudomonas fluorescens strain CHA0 suppresses various plant diseases caused by soil‐borne fungi. The pseudomonad produces the antimicrobial metabolites 2,4‐diacetylphloroglucinol (Phl), pyoluteorin (Plt) and hydrogen cyanide, which are important for disease suppression, as well as the siderophores pyoverdine (Pvd), salicylic acid (Sal) and pyochelin (Pch). In the current work, a derivative of CHA0 with a mutation in the global regulator gene gacA (GacA−), which is unable to produce Phl, Plt and HCN, failed to protect the dicotyledonous plants cress and cucumber against damping‐off caused by Pythium ultimum. In contrast, the GacA− mutant could still protect the Gramineae wheat and maize against damping‐off mediated by the same strain of P. ultimum, and wheat against take‐all caused by Gaeumannomyces graminis. However, the GacA− mutant overproduced Pch and Pvd. To gain more insight into disease protection afforded by the GacA− mutant, a GacA− Pvd− double mutant (strain CHA496) was constructed by gene replacement. Strain CHA496 overproduced Pch and Sal compared with CHA0 and protected wheat against P. ultimum and G. graminis, whereas cress and cucumber were not protected. Addition of FeCl3 repressed Pch and Sal production by strain CHA496 in vitro and impaired the protection of wheat in soil microcosms. In conclusion, a functional gacA gene was necessary for the protection of dicotyledons against root diseases, but not for that of Gramineae. Results indicated also that Pch and/or Sal were involved in the ability of the GacA− Pvd− mutant of CHA0 to suppress root diseases in Gramineae.

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A global regulator of secondary metabolite production in Pseudomonas fluorescens Pf-5

Cited by 145 publications

References 42 publications

Regulation of production of the antifungal metabolite 2,4-diacetylphloroglucinol in Pseudomonas fluorescens F113: genetic analysis of phlF as a transcriptional repressor The GenBank accession number for the sequence reported in this paper is AF129856.

Regulation of production of the antifungal metabolite 2,4-diacetylphloroglucinol in Pseudomonas fluorescens F113: genetic analysis of phlF as a transcriptional repressor The GenBank accession number for the sequence reported in this paper is AF129856.

The global activator GacA of Pseudomonas aeruginosa PAO positively controls the production of the autoinducer N‐butyryl‐homoserine lactone and the formation of the virulence factors pyocyanin, cyanide, and lipase

**The global regulator GacA of Pseudomonas fluorescens CHA0 is required for suppression of root diseases in dicotyledons but not in Gramineae**

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